The effect of vanadyl treatment on vascular responsiveness of streptozotocin-diabetic rats

Abstract

Summary Vanadyl sulphate has been demonstrated to possess insulin-like effects in streptozotocin (STZ) diabetic rats, including the normalization of hyperglycaemia and the prevention of diabetes-induced cardiac dysfunction. However, the effectiveness of vanadyl sulphate on diabetes-related vascular aberrations has not been questioned. Hence, in the present work, we have specifically addressed the question of whether chronic oral vanadyl sulphate treatment has any beneficial effect on diabetes-induced changes in vascular reactivity. Male albino rats were injected with a single intravenous dose of STZ (55 mg/kg). Vanadyl sulphate was administered in the drinking water at a concentration of i mg/ml from 7 days after the STZ injection and treatment was maintained for 10 weeks. Vanadyl intake was accompanied by decreased blood glucose and serum insulin levels. The effects of diabetes on vascular smooth muscle function were assessed by the responsiveness of aortae to noradrenaline and KC1. Contractile responses of the diabetic aortae were found to be significantly increased as compared with controls. However, there were no significant differences in pD2 values of the agonists in either of the groups. Treatment of diabetic rats with vanadyl sulphate completely prevented the increases in responsiveness of aortae to noradrenaline and KC1. The effect of diabetes on the fast and slow components of noradrenaline-induced contraction was also examined. Both components of the response to noradrenaline were significantly increased in diabetic aortae. These changes were also prevented by vanadyl sulphate treatment. The data demonstrate that 10-week vanadyl sulphate treatment results in improved vascular reactivity of diabetic rats. [Diabetologia (1994) 37: 572-578]

Dose‐dependent Effect of Captopril on Aortic Reactivity of Streptozotocin‐diabetic Rats

“…First, the results of the present study demonstrated that endothelium intact and denuded aortic rings from STZ‐diabetic rats are more responsive to the contractile effects of α 1 ‐adrenoceptor agonists like PE than aortic rings from corresponding (non‐diabetic) controls. Similar results showing an increased vascular responsiveness to contractile agents in STZ‐diabetic rats have been reported in previous studies 18,19 . It is well‐known that, in the diabetic state, there is an enhanced oxidative stress due to excessive production of oxygen free radicals and decreased potential of anti‐oxidant defence systems 20,21 .…”

Effect of phenolic acids on functions of rat aorta, vas deferens and on metabolic changes in streptozotocin-induced diabetes

“…[4] It was reported that enhanced contractile responses of STZ-diabetic rat aorta to α-adrenergic agonists as noradrenaline are largely dependent on the presence of extracellular Ca ++ , increased adrenergic stimulation, phosphoinositide metabolism, Ca ++ channels sensitivity, deficiency of endothelial activity and/or decreased calmodulin levels. [16–18] In this study, by evaluation of increased response to PE of STZ-diabetic rat aorta, it was supposed that 6-week STZ-induced diabetes changed the α-adrenergic receptor number and/orthe mechanisms which were mentioned above without changing receptor affinity. However, muscarinic receptor affinity, number or post-receptor pathways remained unchanged.…”

Mechanisms responsible for the vascular effect of aqueous Trigonella foenum-graecum leaf extract in diabetic rats

“…Similar results showing the increased vascular responsiveness to contractile agents in STZ-diabetic rats have been reported in many previous studies. [9–10] This increased vascular smooth muscle responsiveness in diabetic rats could be attributed to deficient endothelial activity,[9–10] enhanced phosphoinositide (PI) metabolism,[11] enhanced sensitivity of calcium channels,[7] and increased sensitivity to adrenergic agonists. [12] Furthermore, oxidative stress is increased due to excessive production of oxygen free radicals and decreased antioxidant defense systems.…”